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Biserni, M.

Publications and source records attributed to Biserni, M..

2 recordsLinked to original sources

Relationship between faecal microbiota and plasma metabolome in rats fed NK603 and MON810 GM maize from the GMO90+ study

Safety concerns arising from the consumption of foods derived from genetically modified (GM) crops remains a highly debated and controversial subject. We report here a faecal microbiota compositional analysis in Wistar rats from the GMO90+ study, which fed glyphosate-tolerant NK603 (+/- Roundup application during cultivation) and Bt toxin MON810 GM maize for 6 months (at 11 and 33% composition of the feed) in comparison to their closest non-GM isogenic lines. We first integrated the faecal microbiota compositional data with results from plasma metabolomics to establish a baseline allowing us to understand which bacterial species can influence host metabolism. Coriobacteriaceae and Acetatifactor significantly predicted plasma metabolic profile in males, while Bifidobacterium and Ruminococcus were able to predict female plasma metabolites. We then investigated the differences in fecal microbiota composition between group of rats fed MON810 or NK603 GM maize varieties in comparison to their respective isogenic lines. Bacterial community richness was not altered by the test diets. There were no statistically significant differences in taxa abundance in the rat faecal microbiota that we could attribute to the consumption of either MON810 or NK603 GM maize varieties. In conclusion, we show that the consumption of the widely cultivated GM maize varieties NK603 and MON810 even up to 33% of the total diet had no effect on the status of the faecal microbiota compared to non-GM near isogenic lines.

molecular biology↗

Integrated transcriptomics and metabolomics reveal signatures of lipid metabolism dysregulation in HepaRG liver cells exposed to PCB 126

Chemical pollutant exposure is a risk factor contributing to the growing epidemic of nonalcoholic fatty liver disease (NAFLD) affecting human populations that consume a Western diet. Although it is recognized that intoxication by chemical pollutants can lead to NAFLD, there is limited information available regarding the mechanism by which typical environmental levels of exposure can contribute to the onset of this disease. Here we describe the alterations in gene expression profiles and metabolite levels in the human hepatocyte HepaRG cell line, a validated model for cellular steatosis, exposed to the polychlorinated biphenyl (PCB) 126, one of the most potent chemical pollutants that can induce NAFLD. Sparse partial least squares classification of the molecular profiles revealed that exposure to PCB 126 provoked a decrease in polyunsaturated fatty acids as well as an increase in sphingolipid levels, concomitant with a decrease in the activity of genes involved in lipid metabolism. This was associated with an increased oxidative stress reflected by marked disturbances in taurine metabolism. A gene ontology analysis showed hallmarks of an activation of the AhR receptor by dioxin-like compounds. These changes in metabolome and transcriptome profiles were observed even at the lowest concentration (100 pM) of PCB 126 tested. A decrease in docosatrienoate levels was the most sensitive biomarker. Overall, our integrated multi-omics analysis provides mechanistic insight into how this class of chemical pollutant can cause NAFLD. Our study lays the foundation for the development of molecular signatures of toxic effects of chemicals causing fatty liver diseases to move away from a chemical risk assessment based on in vivo animal experiments.

pharmacology and toxicology↗